This study seeks: 1. to explore the mechanism of vascular smooth muscle, 2. to characterize those changes occurring in vascular smooth muscle function in association with hypertension, and 3. to determine what role these changes play in the induction and maintenance of DOCA-hypertension in rats. The first hypothesis is that the changes in excitability of isolated helical strips of artery from hypertensive rats is due to an altered binding of calcium by the smooth muscle membrane. In a muscle bath we will inactivate the normal excitation-contraction coupling processes by depolarizing and calcium-depleting the arterial strips and stimulating contraction directly from the contractile machinery by exposure to barium. Plasma calcium concentrations will be chronically raised or lowered by diet. We will measure the responses of helical strips of artery from these rats to determine the effect of altered extracellular calcium levels on excitability. The second hypothesis is that decreased maximum contractility of helical strips of artery from hypertensive rats is due to an increased amount of non-muscular extracellular matter. Biochemical measurements will determine the amount of collagen-elastin and mucopolysaccharides in the arteries of normal and hypertensive rats. Treatment with 17-beta-estradiol or ascorbic acid, respectively, will decrease the content of these substances in the artery. Strip studies will determine the functional effect of arterial content of these extracellular substances on maximum contractility. The third hypothesis is that altered arterial wall composition and contracility are secondary effects of high transmural pressure. Blood pressure in one leg of a rat will be lowered by constricting the major artery supplying the leg. We will determine the contractile response and chemical content of femoral arteries from the protected and unprotected legs of normotensive and DOCA-hypertensive rats to determine the effect of pressure on composition.